α4β2 nicotinic acetylcholine receptors are required for the amyloid β protein-induced suppression of long-term potentiation in rat hippocampal CA1 region in vivo

2008 ◽  
Vol 77 (2-3) ◽  
pp. 84-90 ◽  
Author(s):  
M.N. Wu ◽  
Y.X. He ◽  
F. Guo ◽  
J.S. Qi
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Β Protein ◽  
Term Potentiation

[Gly14]-humanin rescues long-term potentiation from amyloid β protein-induced impairment in the rat hippocampal CA1 region in vivo

Synapse ◽  
2010 ◽  
Vol 64 (1) ◽  
pp. 83-91 ◽  
Author(s):  
Fen Guo ◽  
Wei Jing ◽  
Cun-Gen Ma ◽  
Mei-Na Wu ◽  
Jun-Fang Zhang ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Β Protein ◽  
Term Potentiation ◽  
Hippocampal Ca1

Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo

Nature ◽  
2002 ◽  
Vol 416 (6880) ◽  
pp. 535-539 ◽  
Author(s):  
Dominic M. Walsh ◽  
Igor Klyubin ◽  
Julia V. Fadeeva ◽  
William K. Cullen ◽  
Roger Anwyl ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation

Amyloid-β oligomers: their production, toxicity and therapeutic inhibition

2002 ◽  
Vol 30 (4) ◽  
pp. 552-557 ◽  
Author(s):  
D. M. Walsh ◽  
I. Klyubin ◽  
J. V. Fadeeva ◽  
M. J. Rowan ◽  
D. J. Selkoe
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Specific Form ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation ◽  
Modelling Data

Despite extensive genetic and animal modelling data that support a central role for the amyloid β-protein (Aβ) in the genesis of Alzheimer's disease, the specific form(s) of Aβ which causes injury to neurons in vivo has not been identified. In the present study, we examine the importance of soluble, pre-fibrillar assemblies of Aβ as mediators of neurotoxicity. Specifically, we review the role of cell-derived SDS-stable oligomers, their blocking of hippocampal long-term potentiation in vivo and the finding that this blocking can be prevented by prior treatment of oligomer-producing cells withγ-secretase inhibitors.

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